Abstract

SESSION TYPE: ARDS/Lung Injury Posters

PRESENTED ON: Wednesday, October 24, 2012 at 01:30 PM - 02:30 PM

PURPOSE: Interlukin-2 (IL2) is a proinflammatory cytokine that is a central mediator in systemic inflammation. Recombinant IL-2 is infused during treatment of metastatic melanoma and renal cell carcinoma. Patients receiving high dose IL-2 (HDIL-2) therapy experience systemic inflammation, capillary leak, shock, and acute respiratory failure. Many patients require advanced organ support, including mechanical ventilation. Fulminant organ failure can be avoided by limiting the dose of HDIL-2, but this deprives patients of their treatment for an otherwise terminal disease. There is little data regarding the pathophysiology of respiratory failure during HDIL-2. Our study is to look at changes in pulmonary function throughout the course of HDIL-2 treatment.

METHODS: We studied 5 subjects admitted to the ICU for HDIL-2 (0.6million units/Kg every 8 hours up to 14 doses). Each subject was studied at baseline prior to the first dose of HDIL-2 then daily while in the ICU up to 24 hours after final dose. Each study session included evaluation of spirometry and maximum inspiratory pressure. We also collected daily sequential organ failure assessment (SOFA) scores and laboratory values.

RESULTS: The average forced vital capacity (FVC) was 88.2% (+/- 9.2%) of predicted. By day 2 the FVC declined to 66.4% (+/- 7.2%). FeV1 had similar declines. Two of five subjects had their course terminated because of acute renal failure. Those that continued to receive HDIL-2 had further declines in pulmonary function. However no one required supplemental oxygen. Spirometry inversely correlated with daily SOFA scores, and especially with serum creatinine levels. Spirometry improved within 24hours of drug discontinuation.

CLINICAL IMPLICATIONS: HDIL-2 protocols will benefit from a better understanding of the pathophysiology that leads to organ failure. Spirometry may serve as an early indicator for pulmonary edema. Studies of the progression of organ failure during HDIL-2 may serve as a model for the study of the sepsis.

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